title: Adiponectin modulates DCA-induced inflammation via the ROS/NF-κ B signaling pathway in esophageal adenocarcinoma cells.
abstract: BACKGROUND
  Deoxycholic acid (DCA) promotes the development and progression of esophageal adenocarcinoma (EAC) by inducing inflammation. Adiponectin is reported to have anti-inflammatory and anti-tumor effects.
  
  
  OBJECTIVE
  This study investigated the effects of two types of adiponectin, full-length adiponectin (f-Ad) and globular adiponectin (g-Ad), on DCA-induced inflammation, and investigated the involvement of the reactive oxygen species (ROS)/NF-κB signaling pathway in inflammation in EAC.
  
  
  METHODS
  OE19 cells were treated with DCA (50-300 μM) and/or f-Ad/g-Ad (10.0 μg/ml) or N-acetylcysteine (NAC). The viability of cells exposed to DCA was measured by use of the MTT assay. mRNA and protein levels of the inflammatory factors were examined by real-time PCR and ELISA. Intra-cellular ROS levels were determined by use of flow cytometry. Protein levels of total and p-NF-κB p65 were measured by western blot.
  
  
  RESULTS
  DCA induced dose and time-dependent cytotoxicity. mRNA and protein expression of TNF-α, IL-8, and IL-6 in cells treated with DCA alone were up-regulated, and intra-cellular ROS and p-NF-κB p65 protein levels were also increased. g-Ad promoted inflammatory factor production, ROS levels, and p-NF-κB p65 protein expression whereas f-Ad had a suppressive effect. When combined with DCA, g-Ad enhanced the pro-inflammatory effect of DCA whereas f-Ad, similar to NAC, suppressed the effect.
  
  
  CONCLUSIONS
  DCA has a pro-inflammatory effect in EAC. f-Ad has an anti-inflammatory effect whereas g-Ad seems to have a pro-inflammatory effect in an ROS/NF-κB p65-dependent manner. This indicates that f-Ad could be a potential anti-inflammatory reagent for cancer therapy.
authors.affiliation: Department of Gastroenterology, The Second Affiliated Hospital of School of Medicine, Xi'an Jiaotong University, No. 157, Xi Wu Road, Xi'an, 710004, Shaanxi Province, China.
authors.forename: Rong
authors.initials: R
authors.lastname: Zhang
authors.forename: Xiaoran
authors.initials: X
authors.lastname: Yin
authors.forename: Haitao
authors.initials: H
authors.lastname: Shi
authors.forename: Jie
authors.initials: J
authors.lastname: Wu
authors.forename: Pramod
authors.initials: P
authors.lastname: Shakya
authors.forename: Dong
authors.initials: D
authors.lastname: Liu
authors.forename: Jun
authors.initials: J
authors.lastname: Zhang
mesh_terms: D000230:Adenocarcinoma / Q000737:chemistry / Q000188:drug therapy / Q000517:prevention & control*; D052242:Adiponectin / Q000502:physiology* / Q000627:therapeutic use; D045744:Cell Line, Tumor; D003840:Deoxycholic Acid; D018450:Disease Progression; D004353:Drug Evaluation, Preclinical; D004938:Esophageal Neoplasms / Q000737:chemistry / Q000188:drug therapy / Q000517:prevention & control*; D006801:Humans; D007249:Inflammation / Q000378:metabolism / Q000517:prevention & control; D017382:Reactive Oxygen Species / Q000378:metabolism*; D015398:Signal Transduction / Q000502:physiology*; D051996:Transcription Factor RelA / Q000502:physiology*
chemical_list: D052242:Adiponectin; D017382:Reactive Oxygen Species; D051996:Transcription Factor RelA; D003840:Deoxycholic Acid